Thursday, August 29, 2013

The World Records, that is, not the beer, which always says yes.Two months ago, I posted a blog about "Hendry Vineyard Stickleback", in which I described a paper that my kids (Aspen and Cedar) and I just published:Hendry, A.P., A.S. Hendry, and C.A. Hendry. 2013. Hendry vineyard stickleback: testing for contemporary lake-stream divergence. Evolutionary Ecology Research 15:343-359. PDF-------------------------------------------------------Joacim Naslund added the following comment on the blog:Have you checked if your kids are actually the youngest published scientific authors?

Guinness Book of World Records website states:

"At age 11, Emily Rosa, of Loveland, Colorado, USA, became the youngest person to have research published in a scientific or medical journal when an article she co-authored appeared in the Journal of the American Medical Association on 1 April 1998."

Then, of course, more recently there was the Blackawton Bee study by a class of 8-year olds published in Biology Letters, but your children seem to be even younger.-------------------------------------------------------Who doesn't want to be involved in setting a world record, particularly as a kid. I can certainly remember sitting around and trying to figure out which record I would like to break - and here we had seemingly broken one without even knowing it. So I looked at the Guinness website and found that - yes - according to the record posted there, Aspen (age 10) and Cedar (age 7), should hold the new world record. So why not try? I navigated the Guinness system for submitting a record, added all the proof, and submitted. I didn't pay to have it fast tracked though and so the answer only arrived tonight. Here it is:Thank you for sending
us the details of your proposed record attempt for 'Youngest person to have
research results published'. Here at Guinness World Records we are always
thrilled to hear about new and exciting record breaking proposals.

Unfortunately, after thoroughly reviewing your application with members of our
research team, we are afraid to say that we’re unable to accept your proposal
as a Guinness World Records title.

Our team of expert Records Managers receive thousands of new record proposals
every year from all over the world which are carefully assessed to establish if
they meet our stringent criteria: every record must be measurable by a single
superlative, verifiable, standardisable, breakable and also present an element
of skill.

Whilst we fully appreciate this is not the decision you were hoping for, we
trust that you will understand our position. However, if you have any further
record proposals please do make another application, we would be delighted to
hear from you again.

Once again thank you for contacting Guinness World Records.

Kind regards

XXXXXX XXXXXX

Cedar and Aspen react to the Guinness verdict.

Well, I am not sure who this research team is and why publishing a paper isn't measurable by a single superlative, verifiable, standardisable, breakable and also present an element of skill (as opposed to, say, the longest fingernails or the tallest mohawk or the heaviest onion or the most people to simultaneously apply a facial mask)but there you have it. Maybe I should have paid to have it fast tracked. Or maybe I should take heart in what came after the letter above:If you feel we have
misinterpreted your application, please login on guinnessworldrecords.com
and send us an enquiry clarifying your points, we will then review it and
respond in less than 15 working days.I guess I could clarify by pointing out that Evolutionary Ecology Research is listed in Web of Science and that it has an impact factor over 1.0. I could even send in the anonymous reviews and the Editor's decision letter. How about the data sheets with Aspen's scribbling - or the video of Cedar processing at three years old? Or maybe we should just try again - and quickly. We could published in a journal with a higher impact factor, for example. We could even add someone at Guinness as a co-author. These things we can do - and we can keep trying and trying until we get it right. Very soon, however, I will need a new kid. Better get started on that too.In closing, I would like to reflect on the final paragraph of the Guinness email:Please be aware that as your record application has not been accepted, Guinness
World Records is not associated in any way with the activity relating to your
record proposal and does not endorse this activity in any way. If you choose to
proceed, then this is will be of your own volition and at your own risk.
Guinness World Records will not monitor, measure or verify this activity. I find it sad to think that Guinness does not endorse scientific research - although they are certainly not alone in that respect. Perhaps I can get Aspen or Cedar to start growing their nails.

Saturday, August 24, 2013

I've just had a paper (my first first-author research paper, in fact!) come out in the American Naturalist, and it might be of interest to readers here, so I'll briefly discuss it here. For more, see the article itself (citation and link at bottom).

A "wordle" of this paper. A nice way to see at a glance what the themes of a paper are!

Let me start with a bit of a plug. This research was done at the International Institute for Applied Systems Analysis (IIASA), in Laxenburg, Austria, with my coauthors Ulf Dieckmann and Rupert Mazzucco. I ended up there as a student in their Young Scientists Summer Program (YSSP) in the summer of 2010. That fantastic experience, near the beginning of my PhD at McGill with Andrew, help to lay a conceptual foundation for my PhD thesis on "The role of heterogeneity in adaptation and speciation". It was also simply a wonderful and formative experience, thinking and talking about big issues with a bunch of brilliant fellow students while working in a former summer palace of the Hapsburgs. It was one of the best times I've had in my life – and note that IIASA will be accepting applications for the 2014 YSSP starting this October!

A small part of the schloss, or palace, in Laxenburg where I worked. Marie Antoinette played in the belvedere tower as a child; it is painted with trompe-l'oeil garden scenes, to make the long, cold winters of Austria feel less oppressive. Happily, the YSSP is in the summer! Photo by Ben Haller.

If you want to read a whole lot more about my experiences during the YSSP, you can check out my YSSP blog. And if you want to see lots of photos of my travels in Austria and its vicinity, you can check out my photo album from that time.

OK, enough of that. What of this new paper? For that, I'm actually going to quote a press release I wrote for Am Nat; I wrote it to summarize the paper for a general audience, so it seems perfect to put in this blog, too.

It is imperative that we understand the processes that generate and maintain biodiversity, so that we can more effectively work to conserve that biodiversity for the future. In one such process, called “adaptive divergence”, spatial variation in environmental conditions can promote evolutionary divergence among populations, as each population adapts to its local environmental conditions. This process can ultimately lead to speciation (in sexual organisms) or so-called “evolutionary branching” (in asexual organisms). Previous theoretical work has examined this phenomenon in very abstract, simple environments. However, the effects of more realistically complex patterns of spatial environmental variation, like those found in real landscapes in nature, have never been investigated.

Using a model of asexual organisms inhabiting complex simulated environments, scientists at McGill University and the International Institute for Applied Systems Analysis demonstrate that complex spatial environmental variation can promote evolutionary branching through a novel mechanism they call the “refugium effect”. Refugia are created by patchy environmental variation caused by changes in elevation, moisture, nutrient availability, or any other environmental variable. Organisms that have adapted to conditions elsewhere in a landscape can colonize a refugium and survive there, even though they cannot survive in the harsh environment that surrounds the refugium. For example, an oasis in a desert might act as a refugium for palm trees (and many other organisms). Such patchy environmental variation is omnipresent in real landscapes at all spatial scales.

In the “refugium effect” demonstrated in this research, refugia created by patchy environmental variation can facilitate the evolutionary divergence of populations. Without patchiness, the variation in the environment can be too harsh to allow the organisms to explore, colonize, and adapt to different areas. Refugia due to patchiness can promote such exploration, colonization, and adaptation by providing “stepping-stones” that mitigate the harshness of the environment. This result is important for our understanding of the origins of the vast biodiversity on Earth, since adaptive divergence due to environmental variation is thought to have been a major cause of the biodiversity we see today. This research might also be important to the future conservation of that biodiversity, since it suggests that preservation of environmental variation, not just of “optimal habitat”, might be important to maintaining biodiversity.

That press release emphasizes the "refugium effect" portion of our findings, but there's lots more in the paper as well. In particular, we worked hard to make our model empirically testable, by using metrics of landscape heterogeneity that could be applied to real landscapes. It would be wonderful if some reader of this blog took up that gauntlet and empirically tested our model's findings in some real-world system!

Three views of one run of our model (click to enlarge). Left: a complex landscape, generated by a method that we describe in our paper. Note that there is, broadly, a gradient from red to blue "environment types" across the landscape from left to right, but there is also complex, patchy heterogeneity that has previously not been explored by theoretical models of speciation. Center: A population of organisms that have adapted to local conditions in the environment. Colors of organisms indicate the type of environment in which they are most fit; note that their colors match the color of the environment they inhabit to some extent, due to local adaptation, but that local adaptation is not complete, due to dispersal and stochasticity. Right: The evolutionary history of the population depicted in the center panel, with time proceeding from left to right and phenotype shown on the y-axis (and also using color, as in the other panels). Note the complexity of the evolutionary history; the central green branch (the ancestral type) went extinct, but the landscape can sustain orange and yellow branches that are quite ecologically similar, because of the pattern of heterogeneity in this particular landscape.

We have lots of ideas for extending this research in the future, beginning with making a sexual version of the model to explore how the effects of gene flow and recombination alter our results. To me, it's an exciting area of research that tries to bridge the gap between theoretical and empirical views of speciation. I hope you agree, and thanks for reading!

Thursday, August 15, 2013

At many universities, including McGill, every thesis defense committee must have a “pro-Dean”, who represents the Faculty of Graduate Studies and is responsible for ensuring that the defense is conducted in accordance with university rules and in fairness to the student. The pro-Dean must come from a different faculty than the student, which means that the pro-Dean usually has little or no experience with the topic of the thesis. I am not sure how they normally assign pro-Deans but every once in a while an email goes out asking for emergency pro-Deans. That is, a bunch of thesis defenses are coming up for which they do not yet have pro-Deans arranged – and the email is to ask who might be willing to fill in. The email request usually includes a listing of thesis/departments that need pro-Deans and we are invited to choose one from among them. This allows one to get exposure to different branches of thinking within the university – once I chose to be pro-Dean for a thesis about the spread of militant Islam in western Africa. This time, I could choose between defenses in chemistry, physics, religious studies, medicine, etc. The one from medicine caught my eye: “Translational cancer research: from the bench to the bedside – and back again” by Torsten Holm Nielsen. So I signed up – primarily in the hope of having the opportunity to ask a question that had been in my mind for about six months.

Evolutionary principles are now firmly ensconced in medical research and patient treatment, especially in relation to the evolution of bacterial resistance to antibiotics and viral resistance to antivirals. In particular, the use of any new antibiotic is swiftly followed by the evolution of resistance to that antibiotic, which then necessitates the development of new antibiotics. If this weren’t the case, then penicillin might still be the treatment of choice. The same evolution of resistance is also true for drugs designed to treat HIV. For instance, genome sequencing studies have documented the course of mutations that arise and spread to confer resistance to a given treatment. In both contexts, then, the evolution of resistance alters pathogen population dynamics to allow “evolutionary rescue” in the face of a treatment that would otherwise cause its extirpation from the host. In short, the evolution of resistance by human pathogens provides a clear example of eco-evolutionary dynamics.

In each of the above cases, the first part of the eco-evolutionary problem is evolution by the pathogen population within a given host. To be specific, replication by the pathogen in the host is accompanied by occasional errors (mutations), some of which (by chance) show enhanced resistance to whatever treatment is being applied. As a result, the resistant pathogens show reduced mortality relative to the pathogens without the resistance mutation and, as a consequence, resistance spreads over time through the pathogen population. Eventually, the treatment is no longer effective. The second part of the eco-evolutionary problem is that pathogens that have evolved resistance within one host can spread to new hosts, meaning that a new infection in a new host starts from a position where resistance to the preferred treatment is already strong. This, then, is the two-pronged eco-evolutionary problem faced in the treatment of infectious disease – evolution of resistance within hosts and the transmission of that resistance to new hosts.

I have recently had occasion to re-consider this eco-evolutionary medicine problem from the perspective of cancer. Many years earlier, I had heard several talks about evolution and cancer but my renewed interest came from reading two outstanding books: The Emperor of All Maladies and The Philadelphia Chromosome. Both of these books openly discuss cancer as an evolutionary problem. That is, a tumor is a population of cells in which each (or many) of the cells are replicating out of control – usually as the result of a series of mutations that originally occurred in a line of normal cells. Chemotherapy and radiation therapy are designed to kill these aberrant cells but (hopefully) not normal cells. Sometimes these treatments work right away and sometimes they do not. Other times they work initially but the patient eventually relapses. Both of these limitations are the result of evolution by the cancer cells. During replication by the cancer cells, mutations arise that can (by chance) reduce the cell’s susceptibility to the treatment. As a result – and similar to the first prong of the eco-evolutionary problem discussed above for infectious diseases – the cancer cells without these resistant mutations decrease in proportion relative to the cancer cells with the resistant mutations. During this period, the tumors often shrink as the population of non-resistant cells dies and the patient recovers. Eventually, however, the resistant cells have increased in frequency to the point where they cause expansion of the tumor again.

Cancer biology now has the above evolutionary principles firmly in mind. In particular, tumors are often genetically screened to see what mutations predominate and then treatment is based on chemotherapies known to work best against those mutations – this is the so-called “personalized medicine.” In addition, patients that relapse as their cancer evolves to escape the original treatment are often given a planned subsequent treatment that might better target the newly-evolved resistant cells. Eco-evolutionary cancer medicine!

What struck me when thinking about these phenomena is that – in relation to evolution – cancer is both the same and different from infectious diseases. It is the same with respect to the first prong of the eco-evolutionary problem discussed above – evolution within a patient – but is entirely different with respect to the second problem – transmission to a new person. As far as infectious diseases are concerned, the human body is simply a vehicle for replication and spread to other humans. As far as most cancers are concerned, however, their life – and their genetic line – ends with the death of their host. For cancer then, each human is its own independent world – never to interact with other worlds and with a finite life span beyond which propagation will not be possible. As a result, resistance that evolves within one patient will never (with rare exceptions) be transmitted to another person – which by contrast is the defining feature of infectious diseases.

To me, this suggests that evolutionary applications to cancer treatment will ultimately be very different from those to treat infectious diseases.In cancer, we can – in principle – design a series of effective targeted therapies for the common (and eventually less common) mutations. We can then use those treatments from the get-go, monitor new mutations and treat those with additional targeted therapies, and eventually cure the patient. The unique – and hopeful – part is that the same sequence of treatments should work in the next patient with the same starting mutations – because any resistance that evolved in the first patient will not have transmitted to the next. That is, evolutionary history is reset in each new patient. With infectious diseases, however, the new patient might well be starting from the ending point of the old patient – thus making the personalized treatment protocol much more difficult and the design of new therapies a never ending treadmill.

So this is the idea I wanted to raise at Torsten’s defense. As should be the case for a pro-Dean, I didn’t ask any questions during the defense itself but was encouraged to hear that Torsten and his examiners frequently invoked evolution as a problem faced by cancer therapy. Then, after the committee had asked all of their questions, it was time to ask mine. I gave short description like that above and asked the student if my thinking was crazy. Encouragingly, it seemed it wasn’t. It was also interesting to see – including in discussions later with the committee – that this wasn’t a distinction frequently discussed in cancer therapy. Presumably this is because cancer researchers are not also infectious disease researchers and so they have to deal with the first prong of the eco-evolutionary problem but not the second. Infectious disease researchers on the other hand have not had to think about the first prong in the absence of the second.

The committee was quick to point out some interesting applications of which I was not aware. One particularly interesting one was that some cancer therapies are apparently designed to drive the evolution of the cancer in a particular genetic direction – a direction that can then make it particularly susceptible to another treatment. Kind of like leading the lamb to slaughter or perhaps an evolutionary bait-and-switch. I don’t think this idea is yet in clinical practice but it is seemingly being discussed.

In reality, I suspect that the difference between cancer and infectious diseases probably has been discussed in the literature (perhaps readers of this blog can point out examples) but it was rewarding to have the realization all on my own – and to then have the opportunity to discuss it with the experts. Congratulations Torsten – and good luck in your future endeavors.

------------------------------------------------An aside: In discussions with the committee after the defense, I mentioned reading The Philadephia Chromosome, which is about the development of the first serious targeted cancer therapy for a specific genetic mutation. One of the committee members told me that one of the protagonists of that story – Suzan McNamara – had done a PhD in the laboratory of Dr. Wilson Miller, the person sitting beside me in the defense and the major supervisor for Torsten. In 1998, Suzan developed chronic myelogenous leukemia (CML) and had heard about a targeted cancer treatment in development by Novartis. Novartis was taking the usual careful but glacial steps toward testing their new drug but Suzan and others would die before gaining access. In 1999, Suzan started an online petition that was one of the major pushes causing Novartis to speed up production and testing. Suzan was later featured on advertisements for the drug, which was eventually named Gleevec. Afterward – and I was not aware of this – Suzan decided to become a leukemia researcher, was awarded a PhD in Wilson Miller’s lab, and now works as a clinical trial coordinator at Jewish General Hospital in Montreal – where the defense was taking place. (As a further aside, my uncle also had CML and was enrolled in the early trials of the drug that would become Gleevec. He responded extremely well at first but eventually relapsed and passed away several years later. Nonetheless, Gleevec extended his life and greatly increased its quality.)

Additional personal reasons for an interest in cancer stem from multiple myeloma – on both sides of the family. My mother’s father died of the disease in 1965 and was told at the time that no suitable therapies existed. Then, last year, my father was diagnosed with the same disease, which was my main motivation for reading the two cancer books noted earlier. This time, however, a good targeted therapy existed – bortezomib (Velcade) – a proteasome inhibitor that works by acting on the myeloma cells and the cells with which they interact to inhibit plasma cell growth and reproduction and to promote cell death. In combination with cyclophosphamide (Procytox, Cytoxan), which interferes with the growth and spread of tumor cells, my father is doing very well. I am very grateful for this progress but I can’t help but wish it was present in 1965, in which case I might have been able to meet my grandfather.

Wednesday, August 7, 2013

In August 2012, I had the great fortune to attend the
seventh annual Stickleback meeting, organized by Katie Peichel and held on
Bainbridge Island near Seattle. Here
is the blog I wrote about it.

Since that time, Katie and I have worked to edit the special
issue from the meeting. It appears in my favorite journal Evolutionary Ecology Research.
This post is simply to announce the special issue
and to make everyone aware of its contents. I first repeat the start of our
introductory paper written with great help from Patrik Nosil, Jenny Boughman,
and Blake Matthews. Then I list the full contents with links to each paper.
Enjoy.

From the introductory article “Stickleback research: the now
and the next”

Institutions and programs periodically subject
themselves to progress reports and strategic plans. Flattering summary
statistics are compiled, exciting discoveries are trumpeted, and far-reaching
and ambitious goals and visions are made flesh. At the risk of stretching an
analogy, stickleback have become an institution and research on stickleback has
become a program, and so perhaps it is time for a progress report and strategic
plan. Our goal here is to provide this assessment – or at least a semblance of
it. Although summary statistics are easily compiled (‘stickleback’ appears in
the title of 1846 papersin Web of Science as of 12 March 2013), we prefer to focus on the
state and future of the institution and program by selecting and discussing
several major discoveries (the now) and postulating areas where stickleback are
poised to make important new contributions (the next).

The occasion and excuse for attempting a
progress report and strategic plan for stickleback research was the Seventh
International Conference on Stickleback Behaviour and Evolution hosted by Katie
Peichel in Seattle from 29 July to 3 August 2012. During the course of this
meeting, we heard many talks that summarized the state of various research areas
and that were on the cusp on new and exciting approaches and discoveries. In
discussing these talks, we realized that much could be gained – for us at least
– in summarizing the field and in attempting to prognosticate the future. In
conjunction, Andrew Hendry and Katie Peichel commissioned and edited the
current special issue of Evolutionary
Ecology Research so as to represent the diverse and exciting ideas emerging from
presentations at the Conference.

Thursday, August 1, 2013

In science, multiple possible explanations always exist for any
particular phenomenon. In ideal situations, we can design and perform definitive experiments
that conclusively discriminate between alternative explanations, and thus allow us
to conclusively reject all competing hypotheses save one. This is the best approach for
zeroing in on the true cause of a phenomenon of interest. In many cases, however, definitive experiments are difficult or impossible to perform or - even if they can be performed - remain saddled with considerable ambiguity. That is, multiple competing
hypotheses often remain and cannot be conclusively ruled out through experimental elimination. In such cases, it is customary for investigators to differentially support alternative hypotheses based on circumstantial evidence and assertions as to their plausibility.

A fashionable way to use plausibility to support a given
inference is to invoke parsimony, also known as Occam’s Razor – the idea that (here
citing Wikipedia) “among competing hypotheses, the hypothesis with the fewest
assumptions should be selected. In other words, the simplest explanation is
usually the correct one.” In scientific inference, then, the idea is to
figure out which explanation is the simplest and to then express the greatest
confidence in that hypothesis. To me, this whole enterprise – and the presumption
behind it – is nonsensical, and I have long looked for a venue to express this opinion. A recent visit to Dalhousie University to be an external
examiner for a thesis provided the impetus for me to use this blog as a soap box.

I was the examiner for the thesis of Njal Rollinson, a PhD student of Jeff
Hutchings. Njal had constructed a wonderful thesis using salmonid fishes to
test various adaptive explanations for variation in egg size. Njal's thesis was
one of the better ones that I have examined, with five excellent chapters – all
of them already published in good journals (Ecology, American Naturalist,
Oecologia, EER, and CJFAS). I had a great time reading the thesis because I had studied
this topic in the past and felt that Njal’s work was a great improvement on
previous efforts - including my own. Until I got to the final concluding chapter, that is. In that chapter,
Njal took the courageous approach of arguing that (contrary to the rest of the
thesis) many aspects of egg size variation were not adaptive but instead reflected constraints caused by hard-to-escape genetic correlations.
Reading with raised eyebrows, I then saw that dreaded word – parsimony. In
essence, Njal argued that the simplest argument was that egg
size variation (especially in relation to female size) was not adaptive but
rather a result of genetic correlations between body size and egg
size. He felt that parsimony provided a good basis to make this assertion and to
thereby put adaptive explanations on the back-burner.

1. Who decides which explanation is the simplest –
and by what criteria? What usually happens is that investigators have a
favorite explanation already in mind and find ways to argue that it is the
simplest. But someone else could easily have a different interpretation
regarding simplicity. For instance, genetic drift is often invoked as a more
parsimonious explanation than selection – kind of like a null model that needs
to be rejected before one can invoke the more “complicated” interpretation of
selection[1].
I would argue precisely the opposite. As far as I can tell, no study has
conclusively confirmed genetic drift (as opposed to selection) as a driver of
among-population variation in functional traits – the only sorts of traits for which we would try to infer adaptation anyway[2].
By contrast, countless studies have found strong evidence for adaptive divergence in
such traits. Moreover, adaptation by natural selection is a simple logical (mathematical) outcome
when genetically based traits are related to organismal fitness. Natural selection
thus seems to me a much more parsimonious explanation than drift, which additionally requires very small population sizes and very weak selection! To
paraphrase Bret Weinstein as quoted in The Tapir’s Morning Bath (p. 300):
Adaptation is a better explanation than God, but God is a better explanation
than drift.

2. Who’s to say that nature is parsimonious
anyway? Consider for a moment the frequent use of parsimony as a formal method for
considering the evolution of traits on phylogenetic trees. In essence, the
model of evolution that requires the fewest transitions between character states is
assumed to be the correct one - and this is certainly the simplest (most parsimonious) model. To me this idea seems crazy as a general assumption.
Many cases are known of all sorts of strange, variable, and contradictory
evolutionary changes in a given group of organisms. That is, evolution does not
follow a simple linear progression through a set of states but is instead
rife with all sorts of fits and starts and reversal. So, in this sense, it seems
certain that parsimony will give you the wrong answer. (Although it isn’t
guaranteed that any other methods will give you the right answer).

It was interesting to me that these considerations were
brought back to mind based on arguments about adaptation by natural selection – as opposed to some other scientific question to which parsimony might be applied. It reminded me
of the dark ages of adaptation research – roughly a decade or so following the
publication of Gould and Lewontin’s 1979 paper the “The spandrels of San Marco and
Panglossian paradigm.” That paper
criticized evolutionary biologists for looking only at adaptive explanations
rather than considering non-adaptive ones too. For instance, they pilloried the
approach of “If
one
adaptive argument fails, try another.”Of course, this iterative adaptive approach is precisely what should be done if one wants to get the right answer. Since adaptation is
clearly the most likely explanation for any particular functional trait,
positing and testing one adaptive explanation after another is just the way to
go. (Yes, non-adaptive explanations can be considered too - but certainly not as a null model.)

At this point, it will seem that I am more Panglossian than
even the redoubtable Dr. Pangloss of Voltaire’s Candide, who felt that “everything was for the best in this best of
all possible worlds."[3]
This is certainly not the case as I recognize that constraints can play an important role. To take a caricature, offspring cannot be larger than their
parents at the time of birth - so clearly offspring size is constrained in this inevitable way. Surely this is one case where we can dispense with all attempts
at adaptive explanation and instead chalk up this organismal property to constraint. Or can we? I am reminded of the should-be-classic paper by Norm Ellstrand –
following soon after Gould and Lewontin – titled “Why are juveniles smaller
than their parents?” This paper suggested six adaptive hypotheses for the above-described juvenile
small size (JSS) and marshaled support for each. Buoyed by their success in
postulating adaptive reasons for a very widespread juvenile character, they
suggested:

“Adaptive explanations can be sought for other juvenile
characters as well. In particular, another juvenile character is even more
widespread than JSS and deserves some thoughtful theoretical attention, the
fact that juveniles always seem to be
younger than their parents.”

All these thoughts were going through my head as I examined
Njal and I couldn't help myself from going on a long diatribe along these lines. At the end, I asked Njal “So ... do you agree?” To which he responded “Well,
now that you have brow-beaten me into it.” So, yes, I hope to have also now brow-beaten you into it too. Parsimony is a lousy approach on which to base scientific – and certainly evolutionary – inference, unless of course you believe that
adaptation by natural selection is the most parsimonious explanation.

[1]
Another manifestation of this idea is the testing in time series of phenotypic traits (e.g. fossil data) whether the observed pattern can be distinguished
from a simple model of drift, more specifically a random walk process. The problem with this
approach is that a random walk model can encompass a huge range of possibility
that allows little opportunity for rejection. Moreover, selection is never
consistently directional for extend periods of time and rather jumps around in
fits and starts and reversals – to the extent that many clearly adaptive trends cannot be
distinguished from drift. The solution, of course, is to compare - on an equal
basis (neither model is the null but rather the two are competing
hypotheses) - a drift model and a series of other models, including those based on adaptive mechanisms. Several
papers by Gene Hunt show how this better approach supports adaptation over
drift in many fossil time series.

[2] I did once publish a paper where I argued that drift was the best
explanation for among-population divergence in a trait normally thought to be a
great example of adaptive divergence. I was able to draw this conclusion because I was studying
a situation where selection on that trait was eliminated and so evolution would be
able to proceed by drift. Otherwise, selection will almost always overwhelm
drift. (This paper seems to have been cited only 7 times, when another paper on the same experiment positing adaptive explanations for other traits has been cited 64 times. Sadly, the aforementioned Ellstrand paper has only been cited 5 times.)

[3]
For instance, Dr. Pangloss felt that syphilis was beneficial because it came
from the New World and so was a necessary byproduct of access to New World wonders, such
as chocolate. I can only concur given that I have not had syphilis but have
enjoyed lots of chocolate – moreover I live in the New World.